Pathology and Mineralogy Demonstrate Respirable Crystalline Silica Is a Major Cause of Severe Pneumoconiosis in U.S. Coal Miners

Abstract

Rationale: The reasons for resurgent coal workers' pneumoconiosis and its most severe forms, rapidly progressive pneumoconiosis and progressive massive fibrosis (PMF), in the United States are not yet fully understood. Objectives: To compare the pathologic and mineralogic features of contemporary coal miners with severe pneumoconiosis with those of their historical counterparts. Methods: Lung pathology specimens from 85 coal miners with PMF were included for evaluation and analysis. We compared the proportion of cases with pathologic and mineralogic findings in miners born between 1910 and 1930 (historical) with those in miners born in or after 1930 (contemporary). Results: We found a significantly higher proportion of silica-type PMF (57% vs. 18%; P < 0.001) among contemporary miners compared with their historical counterparts. Mineral dust alveolar proteinosis was also more common in contemporary miners compared with their historical counterparts (70% vs. 37%; P < 0.01). In situ mineralogic analysis showed that the percentage (26.1% vs. 17.8%; P < 0.01) and concentration (47.3 × 10⁸ vs. 25.8 × 10⁸ particles/cm³; P = 0.036) of silica particles were significantly greater in specimens from contemporary miners compared with their historical counterparts. The concentration of silica particles was significantly greater when silica-type PMF, mineral dust alveolar proteinosis, silicotic nodules, or immature silicotic nodules were present (P < 0.05). Conclusions: Exposure to respirable crystalline silica appears causal in the unexpected surge of severe disease in contemporary miners. Our findings underscore the importance of controlling workplace silica exposure to prevent the disabling and untreatable adverse health effects afflicting U.S. coal miners.

Keywords: coal workers; dust; silicosis.

Figure 1.

Flowchart of cases accessioned into the study. PMF = progressive massive fibrosis; RPP = rapidly progressive pneumoconiosis.

Figure 2.

Representative examples of coal, mixed, and silica types of progressive massive fibrosis (PMF) (hematoxylin and eosin stains). (A) Coal-type PMF lesion (⩽25% silicotic nodules). This lesion consists of one large nodule fused to two smaller nodules below. There is substantial collagen with varying orientation surrounded by a rim of coal dust–laden histiocytes with fibrotic extensions into the adjacent parenchyma. There is prominent central necrosis with large quantities of dust. Mature or immature silicotic nodules are not seen, with the possible exception of the small collagenized nodule at bottom left. (B) Mixed-type PMF (>25% and ⩽75% silicotic nodules). This PMF lesion is composed of fused nodules, some with features of coal dust nodules, others showing features of mature silicotic nodules (arrows). Some of the nodules show central necrosis, and there is extensive necrosis with cavitation on the left side of the lesion. Black coal dust pigment is prominent in all areas. (C) Silica-type PMF (>75% silicotic nodules). This lesion is composed almost entirely of mature silicotic nodules. Silicotic nodules are also seen in the adjacent parenchyma with bridging fibrosis (arrow) to the PMF lesion. Black coal mine dust is markedly less apparent than in the other PMF types. Scale bars, 5 mm.

Figure 3.

Immature silicotic nodule. An example of an immature silicotic nodule is shown (hematoxylin and eosin stain). The nodule is composed of central collagen bundles lacking the characteristic central whorling of a mature silicotic nodule. The periphery is composed of fibrohistiocytic cells with prominent lymphocytes. The latter extend into the adjacent lung interstitium. Note that these nodules should not be confused with granulomas, which differ from immature (and mature) silicotic nodules in that they are composed of activated histiocytes and do not have the central collagen bundles. Scale bar, 400 μm.

Figure 4.

Example of MDAP. (A and B) This feature was characterized by the finding of scattered alveoli containing dark pink, finely granular, lipoproteinaceous material (A), which stained with PAS (B). Scale bars: A, 50 μm; B, 60 μm. Characteristic cracking artifact (arrows) was also seen. H&E = hematoxylin and eosin; MDAP = mineral dust–related alveolar proteinosis; PAS = periodic acid–Schiff.